Component

Hepatic retinal oxidase activity

Historical retinal oxidation assay; not assumed identical to a specific modern ALDH isoform.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. A separable aldehyde-oxidase fraction accounted for some NAD-independent retinaldehyde metabolism in human liver and kidney extracts.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/molybdenum-research/10559215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0a70e022e9499ca5d0608c1da80afadfad2215ac6cf1219c8ce8da3280a5238", "start_char": 0, "end_char": 1879, "text_sha256": "a0a70e022e9499ca5d0608c1da80afadfad2215ac6cf1219c8ce8da3280a5238"}
    experimental_model
    Biochemical fractionation of four human livers and three kidneys
    exposure
    Retinaldehyde and other aldehyde substrate assays
    limitations
    Biochemical enzyme-fraction identification predates modern isoform assays; does not establish AOX1 as the dominant human retinoic-acid source or mineral-responsive route.
    nutrient_topic
    Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
    organism
    Homo sapiens
    plain_language
    AOX1 intersects vitamin A chemistry, alongside other enzymes.
    primary_references
    [mo-p10559215] Metabolism of retinaldehyde and other aldehydes in soluble extracts of human liver and kidney. (1999). https://pubmed.ncbi.nlm.nih.gov/10559215/ DOI: 10.1074/jbc.274.47.33366
    tissue_or_cell_type
    Liver and kidney soluble extracts

    Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 885–896

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical fractionation of four human livers and three kidneys · source_derived_draft · unverified_draft

    ### mo-aox-retinal A separable aldehyde-oxidase fraction accounted for some NAD-independent retinaldehyde metabolism in human liver and kidney extracts. Condition category: normal nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: AOX1 intersects vitamin A chemistry, alongside other enzymes. organism: Homo sapiens tissue_or_cell_type: Liver and kidney soluble extracts experimental_model: Biochemical fractionation of four human livers and three kidneys limitations: Biochemical enzyme-fraction identification predates modern isoform assays; does not establish AOX1 as the dominant human retinoic-acid source or mineral-responsive route. exposure: Retinaldehyde and other aldehyde substrate assays evidence_span: {"source_cache": "artifacts/molybdenum-research/10559215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a0a70e022e9499ca5d0608c1da80afadfad2215ac6cf1219c8ce8da3280a5238", "start_char": 0, "end_char": 1879, "text_sha256": "a0a70e022e9499ca5d0608c1da80afadfad2215ac6cf1219c8ce8da3280a5238"} [mo-p10559215] Metabolism of retinaldehyde and other aldehydes in soluble extracts of human liver and kidney. (1999). https://pubmed.ncbi.nlm.nih.gov/10559215/ DOI: 10.1074/jbc.274.47.33366
    Complete structured claim and evidence
  2. The same zinc-deficient rats showed increased retinal oxidase activity, with no detected REH/ARAT activity changes.

    Zinc → Hepatic retinal oxidase activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Same hepatic activity assays.
    limitations
    Activity is not whole-body flux or proof of a direct zinc-binding requirement.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    Vitamin A processing did not simply stop at every step.
    primary_references
    [va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995
    tissue_or_cell_type
    Liver
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1531–1540

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same hepatic activity assays. · source_derived_draft · unverified_draft

    ### va-zinc-deficiency-retinal-oxidation-increase The same zinc-deficient rats showed increased retinal oxidase activity, with no detected REH/ARAT activity changes. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A processing did not simply stop at every step. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Same hepatic activity assays. limitations: Activity is not whole-body flux or proof of a direct zinc-binding requirement. [va-kim1988] Effect of zinc deficiency on hepatic enzymes regulating vitamin A status (1988). https://pubmed.ncbi.nlm.nih.gov/3404291/ DOI: 10.1093/jn/118.8.995
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards